Good afternoon, everyone. My name is Poorna Kannan, and I'm an associate at Needham. Thank you all for joining us this afternoon for Needham's 24th Annual Healthcare Conference. I'm very excited to have with us here today Dr. Christopher Missling, CEO of Anavex Life Sciences, providing a corporate presentation. Dr. Missling, if you're ready, please take it away. Thank you very much for the very kind invitation and kind introduction. We will make a forward-looking statement, so I'd like you to read this. Thank you. We would like to share with you the story of Anavex, where we are. We're dedicated to pushing the boundaries of scientific discovery with novel oral small molecules that are tailored to potentially offer hope and relief. More specifically, we're targeting one of the largest indications right now of unmet medical need, which is Alzheimer's disease and dementia, which is projected to grow over 150 million by 2050. In some countries or regions of the world, it is growing exponentially, with $20 trillion cumulative costs for Alzheimer's and dementia care from 2015 to 2050. One in three Medicare dollars today will be spent in the future on people living with Alzheimer's and other dementias going forward. Eleven million are the numbers of Americans providing unpaid care for people with Alzheimer's and other dementias. Targeting these markets using a differentiated and transformative precision medicine platform is our goal. I'd like to give you an Anavex highlight. We are in the regulatory submission stage with our lead compound, blarcamesine, in the EU with the EMA, which we filed last November and which was accepted a month later in December. We are now in the process of also meeting with other regulatory authorities in order to discuss to proceed with a submission for blarcamesine with early Alzheimer's or Alzheimer's in other regions of the world as well. A quick note about our operations. We are able to fund currently—that's an important subject—our operations for at least four years without additionally raising any cash. We also have no debt. That is also based on the projection on past utilization of our cash utilization rate. We have, with our oral blarcamesine drug, an advantage to currently approved drugs for Alzheimer's disease, early Alzheimer's, Leqembi and Kisunla, which are injectable drugs and require infusion regularly, while our oral drug is given once daily in a more patient-friendly setting at home without the need for moving the patient to a facility or requiring him to observe in a facility for safety updates or safety monitoring with MRIs, which are also inconvenient but also hard to schedule because of the lack of many centers to do that, especially in regions of the rural areas in the Midwest and in rural areas overall. We also have a patent protection for all our product candidates, which is solid. In summary, blarcamesine is a once-daily oral convenient scalable potential treatment for Alzheimer's disease. We not only have Alzheimer's disease as an indication, and we also don't only have blarcamesine as one drug in the company. We also have another drug in the pipeline with clinical data reading out relatively soon, which is Anavex 3-71, which had been now tested in schizophrenia. We're expecting the data—the trial is still ongoing—the data of that study to read out around mid of this year. That is a trial Phase 2 in patients with schizophrenia. The key endpoint is safety as well as biomarker of the EEG with additional clinical measures subsequent. We also have Anavex 3-71, blarcamesine, several formulations. The solid formulation is used for Alzheimer's disease, but we also have a liquid formulation, which is planned for other indications, especially rare diseases where it's harder to swallow for patients who have a harder time to swallow a capsule or a pill, and it's easier to give them a liquid formulation. Again, orally administered candidates offer generally significant potential advantage for clinical benefit relative to costly and logistically challenging biological antibodies-based drugs, which also, as we know, often present additional safety challenges. We believe we are well positioned for expanding this transformative market. Before I go into the details, I'd like to share with you the mechanism, which is very important to understand because it's a differentiated mechanism. It's upstream of what probably targets you used to probably know in the Alzheimer's pathology and other pathologies. We are restoring homeostasis by activating a protein called Sigma-1, which is impaired or has too low expression levels in pathological situations, and the endogenous agonists are not sufficiently available. We can replenish them with the giving of blarcamesine or our drugs. As an outcome, we expect and we see beneficial therapeutic effect for the patient. What's also noteworthy is that if you even have a patient with a mutated Sigma-1 gene, that means the protein is not fully functional, that still works well for the patient to activate it with blarcamesine. In a nutshell, the effect is still powerful, observed for all patients regardless of their genetic standing. We did notice a better outcome for those patients with the Sigma-1 wild type gene, which luckily represents the vast majority with around 70% of the population. Again, all patients benefit from the blarcamesine activation of the receptor. Another important mechanism detail is relevant for Alzheimer's disease specifically, where autophagy, which is an upstream compensatory therapeutic intervention in Alzheimer's, and it's demonstrated by the fact that in the brain, the survival of cells depends on homeostasis balance, restoring functionality, which is extremely complex, the entire brain function. Neurotoxins like A -beta amyloid or tau or inflammation or mitochondrial dysfunction and others are basically, together with the aging, basically pushing back on this homeostasis balance, which the body tries to accomplish. We're able to show that with upstream activation of the Sigma-1 protein with blarcamesine, that can be countered. Just to give you a point of reference, the approach of the antibodies, monoclonal antibodies through an infusion and injection infusion through IV, are trying to downstream to reduce the beta burden in the brain, while oral blarcamesine is doing that more elegantly, upstream and more comprehensively over restoring autophagy activity. As a consequence, not only able to remove these proteins, which are toxic, but also repairing and regenerate and build resilience of the neural cells and the brain function overall. To now move to what are the activities ahead of us, we expect one of the outcomes I mentioned, the schizophrenia top-line data of the Anavex 3-71 Phase 2 study to expect it by the middle of this year. We also expect additional data from the Alzheimer's study Phase 2/3. We did a whole genome exome analysis of the RNA sequence. We like to see if there is a pattern of certain genes which are downregulated in the pathology being restored closer to normal healthy volunteers levels or other genes in the pathology of Alzheimer's disease are changed compared to placebo. We will have a very clear picture of that. Once we have that, we will disclose that, of course. We also plan to initiate several other studies. One of them is a Parkinson's disease study, which will last more than six months and to also subsequently start with two additional studies. One is a Fragile X study and another study of a rare disease, which we have not disclosed yet. We also expect additional publications related to blarcamesine, Anavex 2-73, and Anavex 3-71. We're also expanding the CNS indication with this platform, which comprises blarcamesine, Anavex 2-73, as well as Anavex 3-71, by also looking at potential disease prevention and more about it later. This is the overall population indications we have so far been able to accomplish. It's very much driven by moving towards late stage of trial. This gives you a good overview of the platform potential of blarcamesine and Anavex 3-71, but also other drugs in the pipeline, Anavex 1-41 and Anavex 1066, which are earlier stage. Alzheimer's disease has seen the most trials for blarcamesine with a Phase 1, a Phase 2, and a Phase 2/3 and ongoing open label extension study. We have even compassionate use program ongoing for over nine years. We have ongoing EMA review right now. We also see very nice data for Alzheimer's preclinically with Anavex 3-71, which was published. We also finished a Phase 1 study with 3-71, and that was also published. I want to point out also that the potential future one day is that blarcamesine might be potentially used also prophylactically, given that it's an easy once-daily administration and it's patient-friendly and family-friendly. You don't have to transport the patient anywhere, and it can be used for that reason. We have preclinical data with an animal model of Alzheimer's disease where we gave the drug to the animals before they got sick through Alzheimer's pathology, and they never developed the symptoms of Alzheimer's disease, dementia, or cognitive impairment. While their counterparts, the placebo control, did receive not that benefit. Something interesting down the road and would be an opportunity given it's an oral scalable therapeutic intervention. We are talking about Parkinson's and Parkinson's dementia. We did a Parkinson's dementia proof of concept study, and it was very intriguing because we saw both signals of proof of concept for the cognitive domain of the patients as well as the Parkinsonian domain. We are now deciding how best to proceed with both indications, which have unmet need while Parkinson's is the larger population. The Parkinson's dementia study maybe has more unmet need. We will see how we proceed with both, but we're planning for both indications to move forward. Last but not least, the most advanced clinical trials for a rare disease called Rett syndrome, where we completed three trials. We had also really nice real-world evidence from patients who have been now on the drug for over five years after finishing both placebo-controlled studies as well as the open label studies. They requested to continue to stay on study drug, which the majority have been able to have requested and able to receive accordingly in three regions of the world: in North America, in Europe, as well as in Australia. In totality, there are some patients with Rett syndrome on blarcamesine over five years that is combined open label extension and compassionate use as well. Now let's move to the early Alzheimer's disease trial, which was a 48-week study in three arms, two doses, which were very similar, turned out, and one placebo arm. After 48 weeks, the patients were offered an open label extension of up to 144 weeks. That includes a totality of 192 weeks of analysis, which we will show in a minute. What we found in this placebo-controlled study is an extremely intriguing biomarker response, which is a classical feature of the Alzheimer's pathology, which is shrinking of the brain. As you see on the left side, there's a healthy brain. It's fully and it has hardly any holes. On the right side, you see a brain with Alzheimer's pathology. It has shrunk significantly, and it demonstrates major holes in the middle and on the sides. That is the hallmark of the Alzheimer's brain losing mass of the brain, which, of course, translates also in cognitive impairment and functional impairment. What we found in our trial was a drug-dependent reduction of the atrophy of, which is brain volume loss of almost all regions in the brain of the patients on study drug, which did not happen for patients on placebo. It was in the whole brain and the total gray matter in the parietal lobe, in the temporal lobe, in the limbic lobe, insular cortex, and frontal lobe. Very broad countering the pathology of the Alzheimer's pathology and significantly slowing the atrophy in broad brain regions after 48 weeks of treatment. Now let me move to the open label study, adding to the placebo-controlled the open label blarcamesine treatment. This actually allows for a nice observation or query of how do the patients who got the drug later after they got placebo compare in their cognitive and functional outcome to those who got the drug earlier, which were the patient in the placebo-controlled on blarcamesine to begin with. The group can be separated between continued blarcamesine or also called early start group. In comparison to the patients which switched from placebo to blarcamesine, also referred to as late start group. Let's take a look at what the difference was. First, I'd like to start with the safety. There was a consistent safety profile with no new safety findings for over four years of treatment with blarcamesine. We also were able to address the titration, which was too short in the placebo-controlled study. We expanded it longer in the open label study. This titration adjustment demonstrated the manageable nature of what was the most frequent treatment emergent adverse event, TEAE, which was dizziness, which was reduced more than half to less than 10% in the open label study, demonstrating the manageability just by titration more slowly. Also, very importantly, we did see no deaths related to the study drug in the entire trials. That includes the placebo-controlled as well as the open label study. Regarding the efficacy, we saw that the patients who treated earlier had a significant benefit compared to those patients who had a one-year delay. The difference was for ADAS-COG over 192 weeks up to minus 3.83 points in the ADAS-COG 13, which is an improvement. For ADAS-COG 13, a negative number is an improvement, respectively. For the functional outcome, ADCS-ADL, the difference was 4.3 comparing the earlier start to the late start, which also is an improvement because in activities of daily living, a positive score is an improvement. In totality, the data indicates a disease-modifying effect of oral blarcamesine once daily. In addition to that, the suggested earlier oral blarcamesine treatment initiation may contribute to a continued long-term beneficial therapeutic effect. I also want to point out that a recent publication identifies what is a threshold for a clinically meaningful outcome measure for ADAS-COG. The publication refers to a two-point or larger as a clinically meaningful improvement, which is demonstrated in this data. To look at the chart over time, you see here on the left side the ADAS-COG 13 and on the right side the ADCS-ADL. Left is the cognition and right side the function, respectively. You see nicely the separation between double-blind study and open label extension study. It is interesting that because the trial happened during COVID, there was not like a consistent administration or transition from patients who finished the placebo-controlled study to the open label. In some cases, patients had to wait more than 75 days, some even longer, because they could not go to a hospital to be getting access to the open label extension part of the trial. They had to wait, and they basically didn't get a drug in this period of time. What we learned is that those patients who did not get the drug right away, which were previously on the active arm, they also did not do that well. We learned something in addition to the long-term benefit of blarcamesine compared to a delayed start is that there's also a benefit to not interrupt the treatment of blarcamesine once you start the treatment of blarcamesine. We looked at the literature. That's actually a phenomenon which has been shared by other disease-modifying drugs, which if you take the drug first and then interrupt it for too long, it gets actually worse than if you just never had the drug before and you start the drug. An interesting observation that leads to, again, the conclusion you want to take the drug as early as possible if you have Alzheimer's disease. When you take it, you want to take it continuously and not stop it. This is a lesson which we were able to learn from this phenomenon which happened during COVID. We also want to point out that we published the majority of the study, the placebo-controlled study, in a paper a few months ago in the Journal of Prevention of Alzheimer's Disease. That was demonstrating in totality that the blarcamesine advantage was and is the oral administration. It's a novel target activating autophagy, which is upstream of amyloid beta and tau. For that reason, it might be more closer to the core of the pathology itself and demonstrated promising clinical results. You see on the picture the actual capsules, how they look, which are of blarcamesine. Now I'd like to move to what we're doing in order to prepare for commercial activities. We are very strongly now engaging with patient advocacy, with providers and payers to educate them about blarcamesine in order to build also alliances down the road and build also the case for the advantage of blarcamesine over alternative treatment options. It's important to do that because there is, first of all, an unmet need. The blarcamesine features orally once daily versus challenges of biological antibodies, intravenous drugs needs to be, of course, pointed out in this respect. When we look at the market size, we see that Alzheimer's is the largest market with 6.9 million in the U.S., larger even in Europe with 7 million patients. Asia is even larger, 23. So global, we're talking about 35 million patients currently with this disease of Alzheimer's pathology. Parkinson's disease is a bit smaller with 1 million in the U.S., 1.4 million in Europe, and 10 million global. Schizophrenia has 1.6 million in the U.S., 3 million in Europe, and 24 global. We're addressing really very large markets. You see also the numbers for the respective rare diseases. Want to share briefly about our status on patents. We were very adamant about protecting our composition of matter and other methods of use of our drugs, both Anavex 2-73 as well as Anavex 3-71. In total, we have good patent protection for both candidates up to 2039. That includes composition of matter of blarcamesine, which is very important with a crystallization, which is used and was used in all clinical studies of blarcamesine in Alzheimer's disease specifically. We want to now switch to the commercial and operational status. We believe we have a strong financial profile with at the last quarter of $120.8 million in cash. We have no debt. Last year, the operational expenditures were $30.8 million. We expect it would be a bit higher this year. We can calculate with current cash position that roughly four years of runway. That is a sustainable cash runway, which is also due to disciplined operations and utilizing non-dilutive cash sources that includes cash from non-dilutive funding sources, including the Michael J. Fox Foundation, which we like to thank very much for. I also like to quickly share the team, which consists of senior managers with respective big pharma background. I also like to point out that we have a strong scientific advisory board, which is headed by Marwan Sabbagh, which is the chairman of the scientific advisory board. We continued to get asked to with other candidates, which we might announce soon to add that list, which is already extremely rich and with high-profile physicians and key opinion leaders. With that, I'd like to summarize where we are with Anavex. I want to again emphasize the key advantage of Anavex is the precision medicine platform and its scalability, which allows for equitable and accessible therapeutic intervention for a diverse population and maintaining sustainability within the global healthcare system, which is a challenge these days because every global healthcare system is now looking to reduce cost and cut cost. We would be able to be flexible with a small molecule to address this with our interventions upstream. With that, I'd like to direct you towards more information on our website, www.anavex.com, for more information. I'm excited to keep you in update as we proceed with our programs. Thank you very much. I appreciate it.